Journal
TRENDS IN ENDOCRINOLOGY AND METABOLISM
Volume 21, Issue 1, Pages 41-49Publisher
ELSEVIER SCIENCE LONDON
DOI: 10.1016/j.tem.2009.08.002
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Funding
- Susan Komen Breast Cancer Foundation [BCTR0504227]
- NIH [P30CA56036]
- Dr Ralph and Marian C Falk Medical Research Trust
- Pennsylvania Department of Health
- Margaret Q Landenberger Research Foundation
- [R01CA70896]
- [R01CA75503]
- [R01CA86072]
- [R01CA86071]
- NATIONAL CANCER INSTITUTE [R01CA070896, P30CA056036, R01CA075503, R01CA086072, R29CA070896] Funding Source: NIH RePORTER
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The dachshund (dac) gene was initially described as a mutant phenotype in flies featuring extremely short legs relative to their body length. Functioning as a dominant suppressor of the ellipse mutation, a hypermorphic allele of the Epidermal Growth Factor Receptor (EGFR), the dac gene plays a key role in metazoan development, regulating ocular, limb, brain, and gonadal development. In the Drosophila eye, dac is a key component of the Retinal Determination Gene Network (RDGN) governing the normal initiation of the morphogenetic furrow and thereby eye development. Recent studies have demonstrated an important role for human Dachshund homologue (DACH1) in tumorigenesis, in particular, breast, prostate and ovarian cancer. The molecular mechanisms by which DACH1 regulates differentiation and tumorigenesis are discussed herein.
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